Inhibitory Effect of Apelin on Cardiomyocyte Hypertrophy induced by Resistin in H9c2 Cells

摘要

Background and Objective: Resistin induces cardiac hypertrophy, while apelin inhibits cardiac hypertrophy. But the underlying molecular mechanisms are still not clear that apelin inhibits cardiac hypertrophy induced by resistin. The research purpose was to investigate the underlying molecular mechanism that apelin represses resistin-induced cardiomyocyte hypertrophy. Materials and Methods: H9c2 cells were used to measure surface area of cells and protein synthesis. RT-qPCR was performed to analyze hypertrophic marker brain natriuretic peptide (BNP) and β-myosin heavy chain (β-MHC) mRNA expression. Western blot was employed to examine phosphorylation of LKB1 and AMPK. Results: The results displayed that cell surface area, protein synthesis, BNP and β-MHC mRNA expressions were increased with resistin treatment. While apelin reversed these effects of resistin and this was further blocked by the electrophilic aldehyde lipid peroxidation byproduct 4-hydroxy-2-nonenal (HNE). Furthermore, resistin decreased phosphorylation of LKB1and AMPK, whereas pre-cultured with apelin increased phosphorylation of LKB1and AMPK that was decreased by resistin, which was blocked by HNE. Conclusion: These results suggested that apelin can inhibit cardiomyocyte hypertrophy induced by resistin through the activation of LKB1/AMPK cell signaling pathway.